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Childhood obesity: Current and novel approaches

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The prevalence of childhood obesity has increased over the last fifty years by approximately 5% per decade, and approximately a quarter of all children are now either overweight or obese. These children have a significantly increased risk of many future health problems including adult obesity, type 2 diabetes and heart disease. Despite this relentless increase, common-sense approaches aimed at prevention and treatment have failed to solve the problem. Current approaches at prevention have faced major challenges with some progress in implementing smaller scale programs and social marketing, but little action on broad public policy approaches which often appears unpalatable to society or individual governments. Meanwhile, treatment approaches have mainly focused on lifestyle change, and novel approaches are urgently needed. Prevention needs to shift to improving maternal health prior to conception, with more research focussed on the impact of early years in programming offspring to future overweight/obesity. Likewise, treatment paradigms need to move from simply thinking that obesity can be solved by readdressing diet and activity levels. Novel approaches are needed which take into consideration the complex physiology which regulates early childhood growth and the development of obesity in susceptible individuals.

Introduction

Over the last fifty years, obesity has become a major public health concern, with the majority of adults now being either overweight or obese. Country-specific costs differ but, in Australia, adult obesity was recently estimated to cost the Australian economy $56.6 billion/annum [1]. Alongside this there has been an evolving, and apparently persistently increasing, problem of children and adolescents developing exaggerated early-onset weight gain. Data from the US National Health Examination Survey undertaken in the 1960s indicates that at that time approximately 4–5% of children were overweight [2], [3]. However, since then there has been a steady increase in prevalence, by approximately 5% per decade, in most developed countries [4]. In Australia, the prevalence of overweight and obesity in school-aged children was relatively constant throughout most of the 20th century, but appeared to rise from the 1970s (Fig. 1) [5]. While recent increases appear to have been less dramatic [6], with some reports now even suggesting a plateauing across several countries [7], current figures still indicate that across the developed world >20% of children are now overweight or obese, with America recording rates of approximately 32% [8]. These prevalence data can vary greatly depending upon which cut-points have been selected for analysis (which are mainly World health Organisation, International Obesity Task Force and US Centers for Disease Control and Prevention criteria), but in essence they are all extremely concerning.

Unless there is a sudden and unexpected decline in the prevalence of childhood obesity, which seems very unlikely given that general ‘common sense’ population-based strategies efforts have largely failed to impact on prevalence figures, then large numbers of children and adolescents will grow up to be obese with all of the attendant health risk associated with obesity. Tracking of obesity across the life-course is strong, with most overweight/obese children growing up to be overweight/obese adults. This leads to problems because adult obesity is associated with many health problems, including increased risks of type 2 diabetes, stroke, heart disease, liver and kidney disease as well as a range of different cancers. In fact, a recent study has shown that adults with extreme obesity lose, on average, approximately 14 years of life due to obesity-related comorbidities [9]. However, childhood obesity is also known to have detrimental effects on health. These are both short- and long-term in nature, and include an increased risk of type 2 diabetes, heart and liver disease, obstructive sleep apnoea, joint and mobility issues, and a diverse array of short and long-term psychosocial issues [10].

Approximately 1 in 4 obese children and adolescents have a clustering of cardiovascular risk factors, known as the “metabolic syndrome” [11], and this appears to increase their medium term chance of heart disease by tenfold when compared with healthier children [12]. Furthermore, approximately 10% of obese children have pre-diabetes [11] – a condition which has been shown to progress to type 2 diabetes in the presence of continuing weight gain [13]. While the impact of childhood obesity on life-course mortality is not yet known, mainly because it has not been a problem for long enough to affect the health of older adults, current data paint a bleak picture. Obese adults exhibit reduced life expectancy [14], [15], and the only long-term follow-up study of individuals who developed obesity-related Type 2 diabetes in adolescence found that, within 15 years of diagnosis, one in 20 needed permanent kidney dialysis and one in 10 was dead [16]. Furthermore, obese children and adolescents demonstrate adverse changes in myocardial geometry and function which may predispose to later heart problems [17]. However, we have shown that this course to long-term morbidity and mortality is not set in stone. While the tracking of obesity is strong [18], those individuals who are overweight or obese as a child but grow up to be non-obese adults appear to have the same level of risk for cardiovascular disease and type 2 diabetes as if they had never been overweight [19]. This provides a high level of support for intensive efforts to tackle childhood obesity [20], and it is therefore perhaps not a surprise that increasing efforts are being placed on optimising current approaches to improve effectiveness of prevention and treatment measures. The World Health Organization (WHO) has recently established a high-level Commission on Ending Childhood Obesity [21].

But why hasn't the problem been resolved already? While obesity is based upon the central tenet of a chronic imbalance between energy in and energy out, there are multiple complex social, disease and metabolic networks [22] which lead to compensatory changes that promote weight gain in the face of attempts at change [23].

The environmental causes for obesity are also extremely complex. They include wide-reaching variations in food environment and consumption, physical activity and the environment in which it is undertaken, individual psychology and the society in which individuals exist and interact, and complex biology which regulates weight gain and regulation [24]. On a more specific basis, and within the conceptual framework, there are then variations in personal choices around portion sizes, the purchase of convenience foods, sedentary vs. active living, transport, snacking behaviours, meal routines and the like.

Compounding this, there is also substantial evidence for a strong genetic component to the determination of body composition, especially in young children [25]. In fact, the genetic background of a young child seems much more important than environmental aspects in determining their weight [26]. However, despite enormous advances in genetic technology, there remains a large gap between the evidence for genetic regulation of weight and the number of actual identified weight-regulated genes [27] – a problem that has been coined ‘missing heritability’ [28]. Furthermore, evolving research in the field of epigenetics (relating to heritable changes not caused by actual changes in DNA sequence) suggests that environmental triggers may actually affect the expression of key weight-regulating genes, in a process where our environment moulds our genetic ancestry [29].

Given all of this, it is perhaps therefore not a surprise that single interventions aimed at everything from healthier living at a population level to trials of specific diets or physical activity routines have not led to clear solutions. All, of course, are based on common-sense principles but none have been comprehensive enough, or sufficiently targeted, to achieve sustainable and long-term results ∗[30], ∗[31].

On this background, and given the fact that so many people are overweight/obese or have family members who have been obese and tried different strategies to lose weight, there has then emerged an array of myths and presumptions – many of which have little evidence to substantiate their basis. Presumptions (i.e. persistent beliefs in the absence of supporting scientific evidence) include examples such as ‘regularly eating breakfast protects against obesity’, and ‘snacking contributes to weight gain and obesity’, while myths (i.e. persistent beliefs despite contradictory evidence) includes advice such as ‘slow weight loss has greater long-term benefit than rapid weight loss’, ‘breastfeeding protects against obesity’, and even that ‘sexual activity burns enough calories to aid weight loss’ ∗[32], [33]. Even researchers are not immune from this effect and ‘white hat bias’ in the findings that researchers and/or journal editors/reviewers may subconsciously and selectively promulgate has been a further hindrance to progress [34]. So, where to from here?

Section snippets

Current approaches at prevention

Themes for preventive strategies for tackling childhood obesity often follow the general principles relating to all interventions aimed at preventing health inequalities – namely a) strengthening individuals using person-based educational approaches, b) strengthening communities by building social cohesion and mutual support, c) improving living conditions by reducing exposure to health damaging environments and improving conditions for health, and d) promoting healthy macro policies [35].

Current approaches at treatment

All clinical practice guidelines for the management of childhood obesity focus on diet and activity as mainstays of treatment for those with established obesity [45]. Recommendations include the delivery of support and education to families, rather than children themselves, and via structured programs which are ideally multidisciplinary in nature ∗[46], [47]. On a background of a fairly comprehensive (but still somewhat limited) evidence base [48], they support a comprehensive initial

Novel approaches at prevention

Given evidence that in-utero exposures influence the child's future risk of obesity [59], it is clear that effective prevention of childhood obesity must ideally start prior to conception. As such, addressing a woman's pre-conceptual health, and optimising weight gain during pregnancy with healthy lifestyle measures, is imperative. We [60] and many others [61] have shown the importance of maternal BMI in predicting later health problems in the offspring and there is growing interest in

Novel approaches at treatment

With so many children now being obese, and with evidence that while the prevalence may be plateauing but the level of severity of obesity worsening [85], it is now time to also think of novel ways of treatment if a pandemic of heart disease and type 2 diabetes in the next 20 years is to be avoided.

Some of the novelty around treatment of paediatric obesity may simply come from the trialling of obesity medications which are licensed, or under consideration for licence, in obese adults. These

Summary

In summary, excessive weight gain affects a significant majority of children and, to date, common-sense approaches aimed at prevention and treatment have generally failed to tackle the problem. Emerging evidence highlights the importance of early years in determining risk of future obesity and associated health problems, and yet very little research has been done to investigate the degree to which improvements in maternal peri-conceptual health, infant feeding, weaning and toddler nutrition can

Role of the funding source

Nil.

Conflict of interest statement

Nil.

Acknowledgements

Research at the Murdoch Children's Research Institute is supported by the Victorian Government's Operational Infrastructure Support Program. MAS is supported through The National Health and Medical Research Council (Health Professional Training Fellowship 1012201).

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